The long term objective of these studies has been to evaluate the biochemical basis of the deleterious effects of oxidizing air pollutants with a particular focus on cell membrane effects. The bulk of the studies will use lung phagocytic cells and will evaluate the effect of ozone and nitrogen dioxide on the production of superoxide anion radical, a membrane-associated event; on the fluidity of the plasma membrane; and on the electrochemical potential of the membrane. These studies will include extension of our observation that inhalation of these pollutants results in a decrease in the ability of rat alveolar macrophages to generate superoxide anion radical. Additional studies of this phenomenon will include evaluation of the mechanism of this effort, particularly in relation to lipid peroxidation and to alteration in cell membrane fluidity, and study of whether a similar phenomenon occurs in lung polymorphonuclear leukocytes. Superoxide anion radical generating capability will also be assessed in relation to pollutant effects on phagocytosis and bacteriocidal activity. We also plan to examine whether changes in the dynamic and/or electrochemical properties of phagocyte membranes accompany oxidative damage. This will include determining whether pollutant exposure alters membrane lipid fluidity in intact lung macrophages, circulating granulocytes, and in purified plasma membrane vesicles from alveolar macrophages. In addition, we will investigate the resting stimulation, potential, as well as changes in membrane potential after stimulation, of phagocytic cells from control and pollutant exposed animals.